of light while a trained observer monitors the consensual response of the other pupil under dark conditions. A high scotopic (vision in dim light) threshold indicates low retinal sensitivity, a pathophysiological response to vitamin A deficiency. An early report of pupillary nonresponse to candlelight among night blind Confederate soldiers in the Civil War (Hicks, 1867) led to the development and validation of instrumentation for this test as a reliable, functional measure of vitamin A deficiency in Indonesian (Congdon et al., 1995) and Indian (Sanchez et al., 1997) children. However, data do not currently exist relating pupillary threshold sensitivity as determined by this test to usual vitamin A intakes, and so measures of pupillary response cannot be used at the present to establish dietary vitamin A requirements.

Plasma Retinol Concentration

The concentration of plasma retinol is under tight homeostatic control in individuals and therefore is insensitive to liver vitamin A stores. The relationship is not linear and over a wide range of adequate hepatic vitamin A reserves there is little change in plasma retinol or retinol binding protein (RBP) concentrations (Underwood, 1984). When liver vitamin A reserves fall below a critical concentration, thought to be approximately 20 μg/g of liver (Olson, 1987), plasma retinol concentration declines. When dietary vitamin A is provided to vitamin A-deficient children, plasma retinol concentration increases rapidly, even before liver stores are restored (Devadas et al., 1978; Jayarajan et al., 1980). Thus, a low concentration of plasma retinol may indicate inadequacy of vitamin A status, although median or mean concentrations for plasma retinol may not be well correlated with valid indicators of vitamin A status.

In malnourished populations, often 25 percent or more individuals exhibit a plasma retinol concentration below 0.70 μmol/L (20 μg/dL), a level considered to reflect vitamin A inadequacy in a population (Flores, 1993; Underwood, 1994). However, a low plasma retinol concentration also may result from an inadequate supply of dietary protein, energy, or zinc, all of which are required for a normal rate of synthesis of RBP (Smith et al., 1974). Plasma retinol concentration may also be low during infection as a result of transient decreases in the concentrations of the negative acute phase proteins, RBP, and transthyretin, even when liver retinol is adequate (Christian et al., 1998a; Filteau et al., 1995; Golner et al., 1987; Rosales et al., 1996). The presence of one or more of these factors could lead to an overestimation of the prevalence of vitamin

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